Pouwels-Fry S, Pouwels S, Fournier C, Duchemin A, Tillie-Leblond I, Le Tourneau T, Wallaert B
Clinique des Maladies Respiratoires, Centre de Compétence Maladies Orphelines Pulmonaires, University Hospital, CHRU, Lille, France.
Sarcoidosis Vasc Diffuse Lung Dis. 2008 Dec;25(2):133-9.
Idiopathic pulmonary fibrosis (IPF) is a severe disease with no known effective therapy. Patients with IPF may develop severe increase of pulmonary arterial pressure (PAP) on exercise, the mechanisms of which is not clearly identified.
To determine whether oxygen may correct the increase of PAP developed during exercise in patients with IPF.
We performed a prospective study on patients with IPF and no hypoxaemia at rest. The absence of pulmonary hypertension (PH) at rest was confirmed by echocardiography (systolic PAP <35 mmHg). Eight patients underwent echocardiography during exercise in air and with oxygen (to maintain saturation of at least 94%). Right ventricle-right atrium gradient and cardiac output were measured at rest, after each increment and at peak. We then compared the echocardiographic results obtained for air and oxygen.
All patients developed significant increase of SPAP on exercise (73 +/- 14 mmHg in air). Oxygen did not significantly improve SPAP on exercise (SPAP: 76 +/- 15 mmHg). Echocardiographic characteristics were similar between air and oxygen except for exercise tolerance in term of workload (p=0.045) and endurance (p=0.017). Resting pulmonary function tests did not predict the occurrence of increase of PAP on exercise.
Our results demonstrate that oxygen does not improve exercise-induced increase of PAP in patients with IPF and support the hypothesis that hypoxic vaso-constriction is not the main mechanism of acute increase of PAP during exercise.
特发性肺纤维化(IPF)是一种严重疾病,目前尚无已知的有效治疗方法。IPF患者在运动时可能会出现肺动脉压(PAP)严重升高,但其机制尚不清楚。
确定氧气是否可纠正IPF患者运动时出现的PAP升高。
我们对静息时无低氧血症的IPF患者进行了一项前瞻性研究。通过超声心动图(收缩期PAP<35mmHg)确认静息时无肺动脉高压(PH)。8例患者在空气中运动及吸氧(以维持饱和度至少94%)时接受超声心动图检查。在静息时、每次递增后及峰值时测量右心室-右心房梯度和心输出量。然后比较在空气中和吸氧时获得的超声心动图结果。
所有患者运动时SPAP均显著升高(空气中为73±14mmHg)。吸氧并未显著改善运动时的SPAP(SPAP:76±15mmHg)。除工作量(p=0.045)和耐力(p=0.017)方面的运动耐量外,空气中和吸氧时的超声心动图特征相似。静息肺功能测试无法预测运动时PAP升高的发生。
我们的结果表明,氧气不能改善IPF患者运动诱导的PAP升高,并支持以下假设,即低氧性血管收缩不是运动期间PAP急性升高的主要机制。